000259960 001__ 259960
000259960 005__ 20231004134700.0
000259960 0247_ $$2doi$$a10.1177/23982128231191046
000259960 0247_ $$2pmid$$apmid:37600228
000259960 0247_ $$2pmc$$apmc:PMC10433884
000259960 0247_ $$2altmetric$$aaltmetric:153016306
000259960 037__ $$aDZNE-2023-00813
000259960 041__ $$aEnglish
000259960 082__ $$a610
000259960 1001_ $$aDavies, Caitlin$$b0
000259960 245__ $$aApolipoprotein E isoform does not influence trans-synaptic spread of tau pathology in a mouse model.
000259960 260__ $$aThousand Oaks, CA$$bSage Publishing$$c2023
000259960 3367_ $$2DRIVER$$aarticle
000259960 3367_ $$2DataCite$$aOutput Types/Journal article
000259960 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1694700469_30856
000259960 3367_ $$2BibTeX$$aARTICLE
000259960 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000259960 3367_ $$00$$2EndNote$$aJournal Article
000259960 520__ $$aA key hallmark of Alzheimer's disease (AD) is the accumulation of hyperphosphorylated tau in neurofibrillary tangles. This occurs alongside neuroinflammation and neurodegeneration. Pathological tau propagates through the AD brain in a defined manner, which correlates with neuron and synapse loss and cognitive decline. One proposed mechanism of tau spread is through synaptically connected brain structures. Apolipoprotein E4 (APOE4) genotype is the strongest genetic risk factor for late-onset AD and is associated with increased tau burden. Whether the apolipoprotein E (APOE) genotype influences neurodegeneration via tau spread is currently unknown. Here, we demonstrate that virally expressed human tau (with the P301L mutation) injected into mouse entorhinal cortex at 5-6 months or 15-16 months of age spreads trans-synaptically to the hippocampus by 14 weeks post-injection. Injections of tau in mice expressing human APOE2, APOE3 or APOE4, as well as APOE knock-outs, showed that tau can spread trans-synaptically in all genotypes and that APOE genotype and age do not affect the spread of tau. These data suggest that APOE genotype is not directly linked to synaptic spread of tau in our model, but other mechanisms involving non-cell autonomous manners of tau spread are still possible.
000259960 536__ $$0G:(DE-HGF)POF4-352$$a352 - Disease Mechanisms (POF4-352)$$cPOF4-352$$fPOF IV$$x0
000259960 588__ $$aDataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
000259960 650_7 $$2Other$$aAlzheimer
000259960 650_7 $$2Other$$aapolipoprotein E
000259960 650_7 $$2Other$$aarray tomography
000259960 650_7 $$2Other$$asynapse
000259960 650_7 $$2Other$$atau
000259960 650_7 $$2Other$$atauopathy
000259960 7001_ $$aTulloch, Jane$$b1
000259960 7001_ $$aYip, Ellie$$b2
000259960 7001_ $$aCurrie, Lydia$$b3
000259960 7001_ $$aColom-Cadena, Marti$$b4
000259960 7001_ $$0P:(DE-2719)2812695$$aWegmann, Susanne$$b5$$udzne
000259960 7001_ $$aHyman, Bradley T$$b6
000259960 7001_ $$aWilkins, Lewis$$b7
000259960 7001_ $$aHooley, Monique$$b8
000259960 7001_ $$aTzioras, Makis$$b9
000259960 7001_ $$00000-0003-2530-0598$$aSpires-Jones, Tara L$$b10
000259960 773__ $$0PERI:(DE-600)2889642-7$$a10.1177/23982128231191046$$gVol. 7, p. 23982128231191046$$p23982128231191046$$tBrain and neuroscience advances$$v7$$x2398-2128$$y2023
000259960 8564_ $$uhttps://pub.dzne.de/record/259960/files/DZNE-2023-00813.pdf$$yOpenAccess
000259960 8564_ $$uhttps://pub.dzne.de/record/259960/files/DZNE-2023-00813.pdf?subformat=pdfa$$xpdfa$$yOpenAccess
000259960 909CO $$ooai:pub.dzne.de:259960$$pdnbdelivery$$pdriver$$pVDB$$popen_access$$popenaire
000259960 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2812695$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b5$$kDZNE
000259960 9131_ $$0G:(DE-HGF)POF4-352$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vDisease Mechanisms$$x0
000259960 9141_ $$y2023
000259960 915__ $$0StatID:(DE-HGF)0510$$2StatID$$aOpenAccess
000259960 915__ $$0LIC:(DE-HGF)CCBY4$$2HGFVOC$$aCreative Commons Attribution CC BY 4.0
000259960 915__ $$0StatID:(DE-HGF)0501$$2StatID$$aDBCoverage$$bDOAJ Seal$$d2021-01-15T16:50:32Z
000259960 915__ $$0StatID:(DE-HGF)0500$$2StatID$$aDBCoverage$$bDOAJ$$d2021-01-15T16:50:32Z
000259960 915__ $$0StatID:(DE-HGF)0430$$2StatID$$aNational-Konsortium$$d2023-08-26$$wger
000259960 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2023-08-26
000259960 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2023-08-26
000259960 915__ $$0StatID:(DE-HGF)0320$$2StatID$$aDBCoverage$$bPubMed Central$$d2023-08-26
000259960 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bDOAJ : Anonymous peer review$$d2021-01-15T16:50:32Z
000259960 9201_ $$0I:(DE-2719)1810006$$kAG Wegmann$$lProtein Actions in Neurodegeneration$$x0
000259960 980__ $$ajournal
000259960 980__ $$aVDB
000259960 980__ $$aUNRESTRICTED
000259960 980__ $$aI:(DE-2719)1810006
000259960 9801_ $$aFullTexts